emergency medicine pda
TRANSCRIPT
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Emergency Medicine - Toronto NotesAbridged for the PDA
To be used only in conjunction with the printed Toronto NotesInitial
atient Assessment and Management
Dawn Lim, Chris McColl and Mildred Wong, chapter editors
John Hanlon and Andrea Mok, associate editors
Caroline Collins, EBM editor
Dr. Dan Cass, Dr. Margaret Thompson and Dr. Jeffrey Tyberg, staff editors
Initial Patient Assessment and Management1. Rapid Primary Survey
2. Resuscitation
3. Detailed Secondary Survey
4. Definitive Care
ToxicologyApproach to the Overdose Patient
ABCs of ToxicologyD1- Universal Antidotes
D2 - Draw Bloods
D3 - Decontamination
E - Examine the Patient
G - Give Specific Antidotes and Treatment
Enhanced Elimination
Disposition from the Emergency Department
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1. Rapid Primary Survey (RPS)
Airway maintenance with C-spine control Breathing and ventilation Circulation (pulses, hemorrhage control) Disability (neurological status) Exposure (complete) and Environment (temperature control) restart sequence from beginning if patient deterioratesIMPORTANT: always watch for signs of shock while doing primary survey
A. AIRWAY first priority is to secure airway assume a cervical (C-spine) injury in every trauma patient immobilize with
collar (ER 14) asses ability to breathe and speak ask patient a question; appropriate response indicates patient airway & ability to breathe signs of obstruction
agitation, confusion, universal choking signrespiratory distressfailure to speak, dysphoniaadventitious soundscyanosis
think about ability to maintain patency in future can change rapidly, REASSESS FREQUENTLY (especially if patient status changes)
Airway Management goals
permit adequate oxygenation and ventilationfacilitate ongoing patient managementgive drugs via endotracheal tube (ETT) if IV not available
N.B. start with basic management techniques before progressing to advanced
(see below)
1. Basic Airway Management (Temporizing Measures) protect the C-spine head-tilt chin lift or jaw thrust (if C-spine injury suspected) to open the airway sweep and suction to clear mouth of foreign material nasopharyngeal airway oropharyngeal airway (not if gag present) transtracheal jet ventilation (through cricothyroid membrane)
used as last resort, if unable to ventilate after using above techniques
2. Definitive Airway Management endotracheal intubation (ETI) with inline stabilization of spine (see Figure 1)
orotracheal Rapid Sequence Intubation (RSI)nasotracheal - may be better tolerated in conscious patient
does not provide 100% protection against aspiration contraindicated with basal skull fracture
indications for intubationunable to protect airway (e.g. GCS ? 8; airway trauma)inadequate oxygenation via spontaneous ventilation (O2saturation < 90% with
100% O2or rising pCO2)profound shockanticipate in trauma, overdose, congestive heart failure (CHF), asthma, and
chronic obstructive pulmonary disease (COPD)anticipated transfer of critically ill patients
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surgical airway (if unable to intubate using oral/nasal route)needed for chemical paralysis of agitated patients for investigationscricothyroidotomy
B. BREATHING
LOOK mental status (anxiety, agitation), colour, chest movement (bilateral orasymmetrical?), respiratory rate/effort, nasal flaring, LOC
LISTEN sounds of obstruction (e.g. stridor), breath sounds, symmetry of airentry, air escaping
FEEL flow of air, tracheal shift, chest wall for crepitus, flail segments, suckingchest wounds, subcutaneous emphysema
Breathing Assessment measurement of respiratory function: rate, pulse oximetry, ABG, A-a gradient, peak
flow rate
Management of Breathing treatment modalities:
nasal prongs ^simple face mask ^oxygen reservoir ^CPAP/BiPAPVenturi mask: used to precisely control O2deliveryBag-Valve mask and CPAP: to supplement ventilation
C. CIRCULATION
Definition of Shock inadequate organ and tissue perfusion (brain, kidney, extremities)
Clinical Evaluation rapidly assess for cause of shock clinical features of acute hemorrhage
early: tachypnea, tachycardia, narrow pulse pressure, reduced urine output,
reduced capillary refill, cool extremities and reduced central venouspressure (CVP)late: hypotension and altered mental status
Management of Hemorrhagic Shock secure airway and supply O2TREAT THE CAUSE OF THE SHOCK! control external bleeding
apply direct pressureelevate profusely bleeding extremities if no obvious unstable fractureconsider vascular pressure points (brachial, axillary, femoral)do not remove impaled objects as they tamponade bleedingtourniquet only as last resort
prompt surgical consultation for active internal bleeding infusion of 1-2 L of NS or RL as rapidly as possible replace lost blood volume at ratio of 3:1 (maintain intravascular volume) if inadequate response, consider ongoing blood loss (e.g. chest, abdomen, pelvis,
extremities) ^operative intervention required indications for blood transfusion
severe hypotension on arrivalshock persists following crystalloid infusionrapid bleeding
transfusion options with packed red blood cells (PRBCs)cross-matched (ideal but takes time)type-specific (provided by most blood banks within 10 min.)
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preferred to O-negative uncross-matched blood if both availableO-negative (children and women of child-bearing age)O-positive (everyone else) if no time for cross and matchanticipate complications with massive transfusions
transfusion options with fresh frozen plasma (FFP)used for clinical evidence of impaired hemostasis
ongoing hemorrhage and platelet count < 50,000, PT > 1.5 x normal range vasopressors
used if hypotension persists despite appropriate volume resuscitationdobutamine 2.0-20.0 mcg/kg/min for systolic BP over 100 mmHgdopamine 2.5-20.0 mcg/kg/min for systolic BP 70 to 100 mmHgnorepinephrine 0.5-30.0 mcg/kg/min for systolic BP < 70 mmHg
D. DISABILITY assess level of consciousness by AVPU method (quick, rudimentary assessment) size and reactivity of pupils movement of upper and lower extremities
E. EXPOSURE/ENVIRONMENT undress patient completely essential to assess all areas for possible injury keep patient warm with a blanket radiant heaters; avoid hypothermia
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2. Resuscitation
done simultaneously with primary survey attend to ABCs manage life-threatening problems as they are identified vital signs q 5-15 minutes ECG, BP and O2monitors Foley catheter and nasogastric (NG) tube if indicated order appropriate tests and investigations: may include CBC, lytes, BUN, Cr, glucose,
amylase, INR/PTT, -HCG, toxicology screen, cross & type
3. Detailed Secondary Survey
done after rapid primary survey problems have been addressed intended to identify major injuries or areas of concern head to toe physical exam and X-rays (C-spine, chest, pelvis - required in blunt trauma, consider T-
spine and L-spine)
HISTORY SAMPLE: Signs and Symptoms, Allergies, Medications, Past medical history, Last
meal, Events related to injury
PHYSICAL EXAMINATION
Head and Neck pupils
assess equality, size, symmetry, reactivity to light inequality suggests local eye problem or lateralizing CNS lesion
reactivity/level of consciousness (LOC)
reactive pupils + decreased LOC ^metabolic or structural cause
non-reactive pupils + decreased LOC ^structural cause
extraocular movements and nystagmus fundoscopy (papilledema, hemorrhages) palpation of facial bones, scalp tympanic membranes
Chest inspect for flail segment, contusion palpate for subcutaneous emphysema auscultate lung fields CXR
Abdomen immediate laparotomy if:
refractory shock with no other discernable causeobvious peritonitisincreasingly distended abdomenpositive diagnostic peritoneal lavage, FAST U/S or CT scan
rectal exam for gastrointestinal (GI) bleed, high riding prostate and anal tone (best todo during the log roll)
bimanual exam in females
Musculoskeletal (MSK) examine all extremities for swelling, deformity, contusion, tenderness log roll and palpate thoracic and lumbar spines pelvis: palpate iliac crests and pubic symphysis, pelvic stability (lateral, AP, vertical)
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Neurological Glasgow Coma Scale (GCS) see ER6 alterations of rate and rhythm of breathing are signs of structural or metabolic
abnormalitiesprogressive deterioration of breathing pattern implies a failing CNS
full cranial nerve exam assessment of spinal cord integrity
conscious patient: assess distal sensation and motor abilityunconscious patient: response to painful or noxious stimulus applied to
extremities
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4. Definitive Care
a. continue therapy b. continue patient evaluations (special investigations) c. specialty consultations including O.R. as needed d. disposition: home, admission, or another setting
Hypothermia
predisposing factors: old age, lack of housing, drug overdose, EtOH ingestion, trauma(incapacitating), cold water immersion, outdoor sports
clinical features include: mental confusion, impaired gait, lethargy, combativeness,shivering (eventually stops in severe cases)
may progress to unconsciousness, respiratory depression/arrest, cardiac arrest treatment based on: (a) re-warming and (b) supporting cardiorespiratory function
Re-warming Options Passive External Re-warming (PER):
suitable for most stable patients with core temperature > 32.2Cinvolves covering patient with insulating blanket; body generates heat and
re-warms through metabolic process, shivering Active External Re-warming (AER)
involves use of warming blankets, etc.beware afterdrop phenomenon (warming of extremities causes
vasodilation and movement of cool pooled blood from extremities to core,
resulting in a DROP in core temperature cardiac arrest)safer when done in conjunction with active core re-warming (below)
Active Core Re-warming (ACR)
generally for patients with core temperature
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Approach to the Overdose Patient
History How much? How long ago? What method? (ingestion, inhalation, dermal, ocular,
environmental, IV) accidental vs intentional exposure
Physical Exam focus on: ABCs, LOC/GCS, vitals, pupils
Principles of Toxicology 5 principles to consider with all ingestions
i. resuscitation (ABCs)ii. screening (toxidrome? clinical clues?)iii. decrease absorption of drugiv. increase elimination of drugv. antidote available?
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ABCs of Toxicology
basic axiom of care is symptomatic and supportive treatment address underlying problem only once patient is stable
A Airway (consider stabilizing the C-spine)B BreathingC CirculationD1 Drugs
ACLS as necessary to resuscitate the patient universal antidotes
D2 Draw bloodsD3 Decontamination (decreased absorption, increased elimination)E Expose (look for specific toxidromes)/Examine the PatientF Full vitals, ECG monitor, Foley, x-rays, etc.G Give specific antidotes, treatmentsGo back and reassess.Call Poison Control CentreObtain corroborative history from family
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D1 Universal Antidotes
treatments that will never hurt any patient and may be essential
Oxygen do not deprive an hypoxic patient of oxygen no matter what the antecedent medical
history (i.e. even COPD with CO2retention) if depression of hypoxic drive, intubate and ventilate exception: paraquat or diquat (herbicides) inhalation or ingestion
Thiamine (Vitamin B1) 100 mg IV/IM to all patients with IV/PO glucose a necessary cofactor for glucose metabolism, but do not delay glucose if thiamine
unavailable to prevent Wernicke-Korsakoff syndrome
Wernickes encephalopathy - Ataxia, Confusion, Ophthalmoplegia (WACO)untreated, may progress to Korsakoffs psychosis (disorder in learning and
processing of new information), usually irreversibletreatment: high dose thiamine (1000 mg/day x 3 days)
must assume all undifferentiated comatose patients are at risk
Glucose give to any patient presenting with altered LOC measure blood glucose prior to glucose administration adults: 0.5-1.0 g/kg (1-2 mL/kg) IV of D50W children: 0.25 g/kg (2 mL/kg) IV of D25W
Naloxone antidote for opioids: administration is both diagnostic and therapeutic (1 min onset of
action) used for the undifferentiated comatose patient loading dose
adults 2 mg initial bolus IV/IM/SL/SC or via ETT if no response after 2-3 minutes, increase dose by 2 mg increments until a
response or to max 10 mg known chronic user, suspicious history, or evidence of tracks, give
0.01 mg/kg (to prevent acute withdrawal)child
0.01 mg/kg initial bolus IV/IO/ETT 0.1 mg/kg if no response and narcotic suspected
maintenance dosemay be required because half-life of naloxone much shorter than many narcotics(half-life of naloxone is 30-80 minutes)hourly infusion rate at 2/3 of initial dose that produced patient arousal
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D2 - Draw Bloods
essential bloods (see Table 17 for interpretation)CBC, electrolytes, urea, creatinineglucometer, INR, PTTABGs, measured O2satosmolalityacetylsalicylic acid (ASA), acetaminophen alcohol levels
potentially useful bloodsdrug levels (toxicology screen)Ca2+, Mg2+, PO43protein, albumin, lactate, ketones and liver tests
Serum Drug Levels treat the patient, not the drug level negative tox screen signifies only that the specific drugs tested were not
detectable in the specimen at the time it was obtained (i.e. does not rule outa toxic ingestion)
specific drugs available on general screen vary by institution; check before ordering urine screens also available (qualitative only)
Table 17. Toxic Gaps (see Nephrology,NP16)Anion Gap (AG)= Na+ - (Cl- + HCO3-) normal range 10-14 mmol/L
Metabolic AcidosisIncreased AG: etiologies (* = toxic)MUDPILES CATMethanolUremiaDiabetic ketoacidosis/Starvation ketoacidosisPhenformin*/Paraldehyde*Isoniazid, iron, ibuprofenLactate (anything that causes seizures or shock)Ethylene glycol*Salicylates*Cyanide; carbon monoxide*
Alcoholic Ketoacidosis*Toluene; theophylline*Decreased AG1. error2. electrolyte imbalance (increased Na+/K+/Mg2+)3. hypoalbuminemia (50% fall in albumin
~ 5.5 mmol/L decrease in the AG)4. Li, Br elevation5. paraproteins (multiple myeloma)Normal AG1. K+: pyelonephritis, obstructive nephropathy, renal tubularacidosis (RTA), IV, TPN2. K+: small bowel losses, acetazolamide, RTA I, II
Plasma Osmolar Gap (POG)= measured calculated osmoles normally POG < 10 mOsm/L calculated osmlality = 2Na+ + BUN + blood glucose (mmol/L)
Plasma Osmolar GapsIncreased POG: MAE DIE (if it ends in -ol, it will likely the POG)MethanolAcetoneEthanolDiuretics (glycerol, mannitol, sorbitol)IsopropanolEthylene GlycolOxygen saturation gap= measured calculated O2sat measured by absorption spectrophotometry (pulse oximetry) calculated from Hb/O2saturation curve
Increased O2saturation gap carboxymethemoglobin methemoglobin sulfhemoglobin
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Table 18. Use of the Clinical Laboratory in the Initial Diagnosis of PoisoningTest Finding Selected Causes
ABG hypoventilation (6 pCO2) hyperventilation ( pCO2)
CNS depressants (opioids, sedative-hypnotic agents, phenothiazines, EtOH) salicylates, CO, other asphyxiants
Electrolytes anion-gap metabolicacidosis hyperkalemia
hypokalemia
MUDPILES CAT: see Metabolic Acidosis above digitalis glycosides, fluoride, potassium
theophylline, caffeine, -adrenergic agents, soluble barium salts, diuretics
Glucose hypoglycemia oral hypoglycemia agents, insulin, EtOH
Osmolality andOsmolar Gap
elevated osmolar gap MAE DIE; see Toxic Gaps above
ECG wide QRS complex prolonged QT interval atrioventricular block
TCAs, quinidine, other class Ia and Ic antiarrhythmic agents quinidine and related antiarrhythmics, terfenadine, astemizole Ca2+ antogonists, digitalis glycosides, phenylpropanolamine
Abdominal X-Ray radiopaque pills or objects CHIPES: Calcium, Chloral hydrate, CCl4, Heavy metals, Iron, Potassium,Enteric coated Salicylates, and some foreign bodies
Serum Acetaminophen elevated level(> 140 mg/L or 1000 m/L4 hours after ingestion)
may be only sign of acetaminophen poisoning
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D3 - Decontamination
Ocular Decontamination saline irrigation to neutral pH alkali exposure requires ophthalmology consult
Dermal Decontamination (wear protective gear) remove clothing brush off toxic agents irrigate all external surfaces
Gastrointestinal Decontamination activated charcoal (AC)
indications: single dose will prevent significant absorption of many drugs andtoxins
contraindications: acids, alkalis, cyanides, alcohols, Fe, Lidose = 1 g/kg body weight or 10 g/g drug ingestedodourless, tasteless, prepared as slurry with H2O
cathartics rarely used (risk electrolyte imbalance) whole bowel irrigation
500 mL (child) to 2000 mL (adult) of balanced electrolyte solution/hour bymouth until clear effluent per rectum
indications awake, alert patient who can be nursed upright delayed release product drug/toxin not bound to charcoal drug packages (if any evidence of breakage ^emergency surgery) recent toxin ingestion (up to 4-6 hours)
contraindications evidence of ileus, perforation, or obstruction
surgical removal
indicated for drugs that are toxic, form concretions, or are not removed byconventional means
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E - Examine the Patient
vital signs (including temperature), skin (needle tracks, colour), mucous membranes,odours and CNS
head-to-toe surveyC-spinesigns of trauma, seizures (incontinence, tongue biting, etc.), infection
(meningismus), chronic alcohol/drug abuse (track marks, nasal septum erosion) mental status
Table 19. Specific ToxidromesToxidrome Overdose Signs and Symptoms Examples of Drugs
hyperthermia Hot as a hare antidepressants (e.g. TCAs)
dilated pupils Blind as a bat cyclobenzaprine (Flexeril)
dry skin Dry as a bone carbamazepine
vasodilation Red as a beet antihistamines (e.g. diphenhydramine)
agitation/hallucinations Mad as a hatter antiparkinsonians
ileus The bowel andbladder lose
antipsychotics
urinary retention their tone and theheart
antispasmotics
Anticholinergics
tachycardia goes on alone belladonna alkaloids (e.g. atropine)DUMBELS cholinergic drugs
Diaphoresis, Diarrhea,Decreased blood
pressure
(nicotine,mushrooms)
Urination anticholinesterases
Miosis (physostigmine, organophosphate insecticides)
Bronchospasm,Bronchorrhea,Bradycardia
Emesis, Excitation ofskeletal muscle
Lacrimation
Cholinergics
Salivation, Seizures
dysphonia, dysphagia major tranquilizers
rigidity and tremor antipsychotics
motor restlessness, crawling sensation(akathisia)
constant movements (dyskinesia)dystonia (muscle spasms, laryngospasm, trismus,oculogyric
Extrapyramidal
crisis, torticollis)
Hemoglobin
Derangements
increased respiratory rate carbon monoxide poisoning
decreased level of consciousness (carboxyhemoglobin)
seizures drug ingestion (methemoglobin, sulfhemoglobin)
cyanosis unresponsive to O2
lactic acidosis
Narcotics, Sedatives/ hypothermia EtOH
Hypnotics, EtOH bradycardia, hypotension benzodiazepines
respiratory depression opiates (morphine, heroin, etc.)
dilated or constrictiedpupils (pinpoint inopiate OD)
barbiturates
CNS depressionSympathomimetics increased temperature amphetamines
CNS excitation (including seizures) caffeine
tachycardia, hypertension cocaine, LSD, PCP
nausea and vomiting ephedrine & other decongestants
diaphoresis thyroid hormone
dilated pupils sedative/EtOH withdrawal
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G Give Specific Antidotes and Treatments
Table 20. Protocol for Warfarin OverdoseINR Management< 5.0 reduce maintenance dose hold dose x 1
5.1 9.0 if no risk factors for bleeding, hold warfarin x 1-2 days and reduce maintenance doseOR
if rapid reversal required, Vitamin K 2 4 mg PO, repeat INR in 24 hr
additional Vitamin K 1 2 mg PO if INR still high (onset in 4 6 hr)
9.1 20.0 Vitamin K 3 5 mg PO, INR in 24 hr and additional Vitamin K if necessary
>20.0 fresh frozen plasma (FFP) 10 20 mL/kg
Vitamin K 10 mg IV over 10 min (IV Vitamin K only if life-threatening hemorrhage); onset ~ 2
hr
increase Vitamin K dosing (q4h)
phenobarbital (little evidence)
Table 21. Urine Alkalinization in ASA OverdosePlasma pH Urine pH Treatment
Alkaline Alkaline D5W with 20 mEq KCl/L + 2 amps HCO3-/L at 2 3 cc/kg/hr
Alkaline Acid D5W with 40 mEq KCl/L + 3 amps HCO3-/L at 2 3 cc/kg/hr
Acid Acid D5W with 40 mEq KCl/L + 4 amps HCO3-/L at 2 3 cc/kg/hr
Table 22. Specific Antidotes and TreatmentsToxin Treatment Considerations
Acetaminophen decontaminate often clinically silent; evidence of liver/renal damage delayed >24 hrs
N-acetylcysteine (Mucomyst; useaccording to
toxic dose >= 150 mg/kg (~ 7.0 g)
Rumack-Matthew dosing nomogram) monitor drug level immediately and @ 4 hrs post-ingestion; also liver
enzymes, INR, PTT, BUN, Cr
hypoglycemia, metabolic acidosis, encephalopathy poor prognosis
ASA decontaminate (10:1 charcoal-to-drug ratio)
monitor serum pH and drug levels closely
alkalinize urine (see Table 21); wanturine pH
monitor K+ level; may require supplement for adequate urine
= 7.55 alkalinization
hemodialysis may be needed if intractable metabolic acidosis, very
high levels, or end-organ damage (i.e. unable to diurese)
Anticholinergics supportive care see table 19 for signs and symptoms
Benzodiazepines flumazenil uses for iatrogenic BZ overdose, reversal of BZ sedation
adults: 0.3 mg iv q5min to max1.0g
contraindications: known seizure disorder, mixed OD, and
children: 10ug/kg as above, max0.3 mg
BZ dependence/chronic user
Beta Blockers glucagon: 50-100 ug/kg slow iv push symptoms start within 2 hours of ingestion
(5-10 mg for adults); then 70ug/kg/hr
atropine or isoproterenol if severe
Calcium Channel
Blockers
CaCl 1-4 g of 10% soln iv if BP order ECG, lytes (especially Ca++, Mg2+, Na+, K+)
atropine or isoproterenol if severe
other: high-dose insulin, inotropes or
aggressive supportive therapy
CO Poisoning hyperbaric 100% O2 disputed benefit of hyperbaric O2in mild-moderate cerebral
dysfunction
coma is still undisputed indication for hyperbaric O2
Cyanide lilly Kit (Amyl Nitrate, then NaNitrite): Na thiosulfate
Digoxin decontaminate (charcoal) use for life-threatening arrhythmias unresponsive to
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Digibind (digoxin-specific Abfragments)
conventional therapy, 6 hr serum digoxin >19 nmol/L, initial K+
20 vials if acute; 5-10 if chronic >5mM, ingestion >10 mg (adult) / >4 mg (child)
1 vial (40 mg) neutralizes 0 .6 mg oftoxin
common arrhythmias include V-fib, V-tach, and conduction blocks
Acute DystonicReaction
benztropine: 1-2mg im/iv then 2mg
po x 3 days OR
benztropine (Cogentin) haseuphoric effect and potential for abuse
diphenhydramine 1-2mg/kg iv then
25 mg po qid x 3 days
Heparin protamine sulfate
Insulin/oral
hypoglycemic
glucose iv / po via NG tube glyburide (Diabeta) carries highest risk of hypoglycemia among oral
glucagon: 1-2 mg im (if no access toglucose)
agents; consider octreotide in these cases
Ethanol gastric decontamination if ingestion< 1hr
very common in children (dehydrogenase pathway less active)
thiamine 100 mg im/iv mouthwash = 70% EtOH; perfumes and colognes = 40 - 60% EtOH
manage airway and circulatorysupport
order serum EtOH level and glucose level; treat glucose level
consider hemodialysis if serumEtOH > 500 mg/dL
appropriately
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Enhanced Elimination
Multi-Dose Activated Charcoal (MDAC)
absorption of drug/toxin to charcoal prevents availability and promotes fecalelimination
without charcoal, gut continuously absorbs toxins; MDAC interrupts theenterohepatic circulation of some toxins and binds toxin diffusing back intoenteral membrane from the circulation
MDAC can increase drug elimination (potentially useful for phenobarbitol,carbamazepine, theophylline, digitoxin, others)
dose varies; continue until nontoxic or charcoal stool
EXTRA-CORPOREAL DRUG REMOVAL (ECDR)
Criteria for Hemodialysis toxins that have:
water solubilitylow protein bindinglow molecular weightadequate concentration gradientsmall volume of distribution (Vd) or rapid plasma equilibration
removal of toxin will cause clinical improvement advantage is shown over other modes of therapy predicted that drug or metabolite will have toxic effects impairment of normal routes of elimination (cardiac, renal, or hepatic) clinical deterioration despite maximal medical support useful for toxins at the following blood levels:
alcohols methanol: > 15.6 mmol/L (> 25-50 mg/dL) ethylene glycol: > 8 mmol/L (> 50 mg/dL)
salicylates acute (within 6 h): > 7.2-8.7 mmol/L (> 100 mg/dL) chronic: > 4.3-4.8 mmol/L (> 60 mg/dL)
lithium acute (within 6 h): > 4.0 mmol/L chronic: > 2.5-4.0 mmol/L
bromine: > 15 mmol/Lphenobarbital: 430-650 mmol/L
chloral hydrate (trichloroethanol): > 200 mg/kg others include theophylline, carbemazepine, valproate, methotrexate
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Disposition from the Emergency Department
discharge home vs. prolonged E.D. observation vs. admission methanol, ethylene glycol
delayed onsetadmit and watch clinical and biochemical markers
TCAsprolonged/delayed cardiotoxicity warrants admission to monitored (ICU)
bedif asymptomatic and no clinical signs of intoxication: 6 hour E.D. observationadequate with proper decontaminationsinus tachycardia alone (most common finding) with history of OD warrants
observation in E.D. hydrocarbons/smoke inhalation
pneumonitis may lag 6-8 hoursconsider observation for repeated clinical and radiographic examination
ASA, acetaminophenif borderline level, get second level 2-4 hours after first
oral hypoglycemicsadmit all patients for minimum 24 hours if hypoglycemic
Psychiatric Consultation once patient medically cleared, arrange psychiatric intervention if required beware - suicidal ideation may not be expressed